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{{Pre-eclampsia}}
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==Overview==
Common causes of [[preeclampsia]] include [[uteroplacental ischemia]] and [[genetic]] predisposition following the formation of [[atheromatous plaques]] and [[fibrinoid necrosis]] of the [[spiral]] [[vessel walls]], [[oxidative stress]] in [[trophoblast cells]], [[apoptosis]] in [[trophoblast cells]],[[systemic inflammatory response]], [[vasospasm]], [[platelet]] aggregation, [[thrombin]] formation, deposition of the [[fibrin]] in multiple [[organs]].


Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753; Stacie Zelman, M.D. [2]; Associate Editor(s)-In-Chief: Ogheneochuko Ajari MB.BS, MS
==Causes==
==Causes==
The pre-eclampsia syndrome is thought in some cases to be caused by a shallowly implanted placenta which becomes hypoxic, leading to upregulated [[inflammatory]] mediators secreted by the [[placenta]] and acting on the vascular [[endothelium]].  The shallow implantation is thought to stem from the maternal system's response to the placenta. But in some cases of preeclampsia, the placenta appears to have implanted normally. Possibly women with higher baseline levels of inflammation stemming from underlying conditions such as chronic hypertension may have normally implanted placentae, but less tolerance for the inflammatory burden of pregnancy.
Common cause of [[preeclampsia]] include [[uteroplacental]] [[ischemia]] and [[genetic predisposition]] due to the following:<ref name="LyeBloise2013">{{cite journal|last1=Lye|first1=P.|last2=Bloise|first2=E.|last3=Dunk|first3=C.|last4=Javam|first4=M.|last5=Gibb|first5=W.|last6=Lye|first6=S.J.|last7=Matthews|first7=S.G.|title=Effect of oxygen on multidrug resistance in the first trimester human placenta|journal=Placenta|volume=34|issue=9|year=2013|pages=817–823|issn=01434004|doi=10.1016/j.placenta.2013.05.010}}</ref><ref name="MayrinkCosta2018">{{cite journal|last1=Mayrink|first1=J.|last2=Costa|first2=M. L.|last3=Cecatti|first3=J. G.|title=Preeclampsia in 2018: Revisiting Concepts, Physiopathology, and Prediction|journal=The Scientific World Journal|volume=2018|year=2018|pages=1–9|issn=2356-6140|doi=10.1155/2018/6268276}}</ref>
 
If severe, preeclampsia progresses to ''fulminant pre-eclampsia,'' with [[headache]]s, visual disturbances, and epigastric pain, and further to [[HELLP syndrome]] and[[eclampsia]]. [[Placental abruption]] is associated with hypertensive pregnancies. These are [[medical emergency|life-threatening conditions]] for both the developing baby and the mother.
* The formation of [[atheromatous plaques]] and [[fibrinoid necrosis]] of the [[spiral]] [[vessel walls]]
 
* [[Oxidative stress]] in [[trophoblast cells]]
Many theories have attempted to explain why the preeclampsia syndrome arises in some pregnancies:
* [[Apoptosis]] in [[trophoblast cells]]
* vitamin D deficiency  J Clinical Endorcinol Metabolism  Sept 2007  92(9) 3517-22
* [[Systemic inflammatory response]]
* endothelial cell injury
* [[Vasospasm]]
* rejection phenomenon
* [[Platelet]] aggregation
* compromised placental perfusion
* [[Thrombin]] formation
* altered vascular reactivity
* Deposition of the [[fibrin]] in multiple [[organs]]
* imbalance between prostacyclin and thromboxane
* decreased glomerular filtration rate with retention of salt and water
* decreased intravascular volume
* increased central nervous system irritability
* disseminated intravascular coagulation
* uterine muscle stretch (ischemia)
* dietary factors
* genetic factors<ref name=AMN>{{cite web | author =Courtney Reynolds, MD, William C. Mabie, MD, & Baha M. Sibai, MD | title =Preeclampsia | publisher=Armenian Medical Network |work =Pregancy - Hypertensive Disorders | url=http://www.health.am/pregnancy/preeclampsia/ | year = 2006 | accessdate=2006-11-23}}</ref>
 
The current understanding of the disease is as a two-stage process, with a variable first stage which predisposes the placenta to hypoxia, followed by the release of soluble factors which result in many of the other observed phenomena.  Many of the older theories can be subsumed under this umbrella, as the soluble factors have been shown to cause, for example, endothelial cell injury, altered vascular reactivity, the classic lesion of glomerular endotheliosis, decreased intravascular volume, etc.  Underlying maternal susceptibility to the damage is likely implicated as well.


==References==
==References==
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[[Category:Emergency medicine]]
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[[Category:Cardiology]]
[[Category:Cardiology]]
 
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Latest revision as of 14:51, 4 March 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Ogheneochuko Ajari, MB.BS, MS [3]

Overview

Common causes of preeclampsia include uteroplacental ischemia and genetic predisposition following the formation of atheromatous plaques and fibrinoid necrosis of the spiral vessel walls, oxidative stress in trophoblast cells, apoptosis in trophoblast cells,systemic inflammatory response, vasospasm, platelet aggregation, thrombin formation, deposition of the fibrin in multiple organs.

Causes

Common cause of preeclampsia include uteroplacental ischemia and genetic predisposition due to the following:[1][2]

References

  1. ↑ Lye, P.; Bloise, E.; Dunk, C.; Javam, M.; Gibb, W.; Lye, S.J.; Matthews, S.G. (2013). "Effect of oxygen on multidrug resistance in the first trimester human placenta". Placenta. 34 (9): 817–823. doi:10.1016/j.placenta.2013.05.010. ISSN 0143-4004.
  2. ↑ Mayrink, J.; Costa, M. L.; Cecatti, J. G. (2018). "Preeclampsia in 2018: Revisiting Concepts, Physiopathology, and Prediction". The Scientific World Journal. 2018: 1–9. doi:10.1155/2018/6268276. ISSN 2356-6140.
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